Effects of endothelin-1 on the membrane potential and slow waves in circular smooth muscle of rat gastric antrum

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Electrophysiological effects of endothelin-1 (ET-1) on circular smooth muscle of rat gastric antrum were investigated by using intracellular membrane potential recording techniques. ET-1 (10 nM) caused an initial hyperpolarization of the membrane which was followed by a sustained depolarization. ET-1 also increased the frequency but not the amplitude of slow waves. In the presence of the endothelin type A (ET_A) receptor antagonist, BQ123 (1 μM), ET-1 (10 nM) depolarized the membrane and increased the frequency of slow waves, but without the initial hyperpolarization. The selective endothelin type B (ET_B) receptor agonist, sarafotoxin S6c (10 nM), also depolarized the membrane and increased the frequency of slow waves. In the presence of the ET_B receptor antagonist, BQ788 (1 μM), ET-1 (10 nM) hyperpolarized the membrane. However, in the presence of BQ788, ET-1 caused neither the depolarization nor the increase in the frequency of the slow waves. The ET-1-induced hyperpolarization was completely abolished by apamin (0.1 μM). In the presence of apamin, ET-1 depolarized the membrane and increased the frequency of slow waves. The ET-1-induced depolarization was significantly attenuated by 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS, 0.3 mM). The increase of the frequency by ET-1 was observed both in the presence and absence of DIDS. These results suggest that, ET-1 hyperpolarizes the membrane by the activation of Ca<2+>-activated K^+ channels via ETA receptors, and depolarizes the membrane by the activation of Ca^<2+>- activated C^- channels via ET_B receptors. ET-1 also appears to increase the frequency of slow waves via ET_B receptors, however this mechanism would seem to be independent of membrane depolarization.
日本平滑筋学会の論文

Effects of endothelin-1 on the membrane potential and slow waves in circular smooth muscle of rat gastric antrum

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